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Journal articles on the topic 'Ph-negative chronic myeloproliferative neoplasms'

Author: Grafiati

Published: 9 March 2023

Last updated: 19 July 2025

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1

Мурзабекова, М. А., Я. М. Марченко, Д. И. Шихбабаева, and О. Ю. Виноградова. "Genetic Aspects Classical Ph-negative Myeloproliferative Neoplasms (Literature Review)." Гематология. Трансфузиология. Восточная Европа 10, no. 2 (2024): 210–18. http://dx.doi.org/10.34883/pi.2024.10.2.001.

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Рh-негативные миелопролиферативные новообразования – это группа заболеваний, которые характеризуются клональной пролиферацией одной или нескольких клеточных линий миелоидных предшественников, а также соединительнотканных компонентов костного мозга и сопровождаются изменениями показателей крови. В соответствии с классификацией Всемирной организации здравоохранения 2022 года к Ph-негативным новообразованиям относятся истинная полицитемия, эссенциальная тромбоцитемия, первичный миелофиброз, хронический нейтрофильный лейкоз, хронический эозинофильный лейкоз, ювенильный миеломоноцитарный лейкоз и м

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2

Martinkov, V. N., D. K. Novik, I. V. Veyalkin, A. E. Silin, and I. A. Iskrov. "The incidence of Ph-negative chronic myeloproliferative neoplasms in Belarus." Russian journal of hematology and transfusiology 68, no. 3 (2023): 363–72. http://dx.doi.org/10.35754/0234-5730-2023-68-3-363-372.

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Introduction. Ph-negative myeloproliferative neoplasms (MPN) are chronic clonal disorders characterized by the proliferation of mature cells from one or more myeloid cell lines. These disorders include polycythemia vera (PV), essential thrombocythemia (ET), and primary myelofibrosis (PMF). The incidence of classical Ph-negative MPN varies significantly throughout the world. These differences may be due to geographical or population features, as well as due to differences in methods of diagnosis and recording. Aim: to determine incidence of Ph-negative MPN in Belarus. Materials and methods. Dat

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3

Polyakov, A. S., V. V. Tyrenko, Ya A. Noskov, D. K. Zhogolev, and A. V. Kovalev. "Clinical and laboratory features of different types of interferon therapy classic Ph-negative myeloproliferative neoplasms." Genes & Cells 11, no. 3 (2016): 153–61. http://dx.doi.org/10.23868/gc120618.

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Chronic myeloproliferative neoplasms are a group of disorders characterized by clonal disturbance of pluripotent bone marrow stem cells, leading to an excessive increase in hematopoietic cells that retain the ability to differentiate. Modern screening techniques have made changes to the current view of the epidemiology of myeloproliferative neoplasms. Recently, more and more researches are found with the median age below 50 years, and sometimes less than 40 years. This circumstance determines the need to improve therapy with the use of interferon-а. A new stage in the treatment of myeloprolife

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4

Bittencourt, Rosane Isabel, Jose Vassallo, Maria de Lourdes Lopes Ferrari Chauffaille, et al. "Philadelphia-negative chronic myeloproliferative neoplasms." Revista Brasileira de Hematologia e Hemoterapia 34, no. 2 (2012): 140–49. http://dx.doi.org/10.5581/1516-8484.20120034.

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5

Tarakanova, A. V., D. S. Abramov, A. V. Pshonkin, and D. M. Konovalov. "Pathomorphological diagnosis of Ph-negative chronic myeloproliferative neoplasms in children." Pediatric Hematology/Oncology and Immunopathology 23, no. 3 (2024): 123–29. http://dx.doi.org/10.24287/1726-1708-2024-23-3-123-129.

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BCR::ABL/Ph-negative chronic myeloproliferative neoplasms (CMPN) in children differ from those in adults in clinical manifestations and genetic alterations. Taking into account the well-known physiology of hematopoiesis in children, it seems important to compare the histological features of CMPN in pediatric patients with the criteria for the diagnosis of these diseases in adults specified in the World Health Organization (WHO) classification. In pediatric practice, the interpretation of changes in hematopoiesis in patients with CMPN without any established driver mutation has a particular imp

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6

Ryabukhina, Yu E., P. A. Zeynalova, O. I. Timofeeva, et al. "Combination approach to diagnosis and treatment of an elderly patient with chronic Ph-negative myeloproliferative neoplasm and concomitant surgical pathology. Clinical observation." MD-Onco 1, no. 1 (2021): 61–65. http://dx.doi.org/10.17650/2782-3202-2021-1-1-61-65.

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Chronic myeloproliferative neoplasms (CMPN), Ph-negative, are of clonal nature, develop on the level of hematopoietic stem cell and are characterized by proliferation of one or more hematopoietic pathways. Currently, the group of Ph-negative CMPN includes essential thrombocythemia, primary myelofibrosis, polycythemia vera, myeloproliferative neoplasm unclassifiable.Identification of mutations in the Jak2 (V617F), CALR, and MPL genes extended understanding of biological features of Ph-negative CMPN and improved differential diagnosis of myeloid neoplasms. Nonetheless, clinical practice still en

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7

Hasserjian, Robert P. "The spectrum of Ph-negative disease: CNL and CSF3R-related disorders." Hematology 2024, no. 1 (2024): 270–78. https://doi.org/10.1182/hematology.2024000555.

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Abstract Chronic neutrophilic leukemia (CNL) is a very rare myeloid neoplasm characterized by peripheral blood neutrophilia and a hypercellular marrow with increased granulopoiesis. An activating mutation in CSF3R is present in 80% to 90% of cases. CNL displays some biological overlap in terms of clinical presentation and behavior, as well as genetic profile, with several other myeloid neoplasms, particularly myelodysplastic/myeloproliferative neoplasms (MDS/MPN) and other MPN. Distinguishing these related entities can be challenging, requires close attention to peripheral blood and bone marro

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8

Nann, Dominik, and Falko Fend. "Synoptic Diagnostics of Myeloproliferative Neoplasms: Morphology and Molecular Genetics." Cancers 13, no. 14 (2021): 3528. http://dx.doi.org/10.3390/cancers13143528.

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The diagnosis of a myeloid neoplasm relies on a combination of clinical, morphological, immunophenotypic and genetic features, and an integrated, multimodality approach is needed for precise classification. The basic diagnostics of myeloid neoplasms still rely on cell counts and morphology of peripheral blood and bone marrow aspirate, flow cytometry, cytogenetics and bone marrow trephine biopsy, but particularly in the setting of Ph− myeloproliferative neoplasms (MPN), the trephine biopsy has a crucial role. Nowadays, molecular studies are of great importance in confirming or refining a diagno

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9

Polushkina, Lyubov, Irina Martynkevich, Vasily Shuvaev, et al. "Genetic and Epigenetic Alterations of Ph-Negative Myeloproliferative Neoplasms." Blood 124, no. 21 (2014): 5549. http://dx.doi.org/10.1182/blood.v124.21.5549.5549.

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Abstract Objectives and background: Genetic mutations result in abnormalities of myelopoietic proteins and lie in the basis of Ph-negative myeloproliferative neoplasms (MPNs) development and its subsequent progression. Several somatic mutations in JAK2, MPL, TET2, EZH2, ASXL1, CBL, IDH1, IDH2, IKZF1 genes were detected in chronic and blastic phase MPNs. Recent studies have revealed a number of epigenetic alterations that contribute to Ph-negative MPNs pathogenesis and determine the clinical outcome. Mutations involving the EZH2 gene are thought to result in loss of methyltransferase activity s

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10

Paciaroni, Katia, Selenia Campagna, Nicoletta Villiva', et al. "CO-OCCURRENCE OF JAK2/CALR-POSITIVE MYELOPROLIFERATIVE DISORDER AND BCR-ABL-POSITIVE CHRONIC MYELOGENOUS LEUKAEMIA TREATED WITH COMBINATION OF TYROSINE KINASE INHIBITORS AND RUXOLITINIB." Mediterranean Journal of Hematology and Infectious Diseases 17, no. 1 (2025): e2025023. https://doi.org/10.4084/mjhid.2025.023.

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The concomitant presence of BCR-Abl1 and JAK2/CALR mutations in Myeloproliferative neoplasms (MPNs) is rare. The clinical presentation of Chronic Myelogenous Leukemia (CML) and Ph-negative MPN may vary, but CML seems to play a dominant role, so patients usually receive treatment with tyrosine kinase inhibitor (TKI) only. The second Ph-negative MPN becomes evident under the selective pressure of the TK.I.

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11

Lindholm Sørensen, Anders, and Hans Carl Hasselbalch. "Smoking and philadelphia-negative chronic myeloproliferative neoplasms." European Journal of Haematology 97, no. 1 (2015): 63–69. http://dx.doi.org/10.1111/ejh.12684.

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12

Cazzola, Mario, Luca Malcovati, and Rosangela Invernizzi. "Myelodysplastic/Myeloproliferative Neoplasms." Hematology 2011, no. 1 (2011): 264–72. http://dx.doi.org/10.1182/asheducation-2011.1.264.

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Abstract According to the World Health Organization (WHO) classification of tumors of hematopoietic and lymphoid tissues, myelodysplastic/myeloproliferative neoplasms are clonal myeloid neoplasms that have some clinical, laboratory, or morphologic findings that support a diagnosis of myelodysplastic syndrome, and other findings that are more consistent with myeloproliferative neoplasms. These disorders include chronic myelomonocytic leukemia, atypical chronic myeloid leukemia (BCR-ABL1 negative), juvenile myelomonocytic leukemia, and myelodysplastic/myeloproliferative neoplasms, unclassifiable

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13

Novik, D., V. Martinkov, I. Veyalkin, et al. "Regional features of the incidence of chronic Ph-negative myeloproliferative neoplasms in Belarus." Medical and Biological Problems of Life Activity, no. 1 (May 22, 2023): 67–74. http://dx.doi.org/10.58708/2074-2088.2023-1(29)-67-74.

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According to published data, there are differences in the registered incidence of chronic Ph-negative myeloproliferative neoplasms (MPN) in some regions of the world. In this study, for the first time, we compare the Ph- MPN incidence in the regions of Belarus in order to determine the regional features.It was shown that for the period 2014-2018 the highest rates of standardized incidence of polycythemia vera were noted in the Brest region – 1,17 and Minsk – 1,11, the lowest incidence rate was determined in the Vitebsk region – 0,68 per 100,000 population per year, p<0,05. The maximum incid

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14

Santos, Fabio P. S., Renato D. Puga, Ricardo Helman, et al. "Whole Exome Sequencing of Philadelphia-Negative (Ph-negative) Myeloproliferative Neoplasms (MPNs) and Myelodysplastic/Myeloproliferative Disorders (MDS/MPD)." Blood 124, no. 21 (2014): 4593. http://dx.doi.org/10.1182/blood.v124.21.4593.4593.

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Abstract Introduction: The development of next-generation sequencing has made it feasible to interrogate the entire genome or exome (coding genome) in a single experiment. Accordingly, our knowledge of the somatic mutations that cause cancer has increased exponentially in the last years. MPNs and MDS/MPD are chronic myeloid neoplasms characterized by an increased proliferation of one or more hematopoietic cell lineages, and an increased risk of transformation to acute myeloid leukemia (AML). MPNs and MDS/MPDs are heterogenous disorders, both in clinical presentation and in prognosis. We sought

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15

Shuvaev, Vasily, Irina Martynkevich, Alla Abdulkadyrova, et al. "Ph-Negative Chronic Myeloproliferative Neoplasms – Population Analysis, a Single Center 10-years’ Experience." Blood 124, no. 21 (2014): 5556. http://dx.doi.org/10.1182/blood.v124.21.5556.5556.

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Abstract Objectives and background. Nowadays chronic myeloproliferative neoplasms (MPN) other than chronic myelogenous leukemia undergo renaissance of interest. It results from advances in decryption of molecular mechanisms of pathogenesis and invention of target drugs. Epidemiological information is needed to assess potential effect and additional costs of new diagnostic and therapeutic techniques. The objective of our study was to review experience of MPN diagnostic and treatment in our center for past ten years. Methods. Our institution serves as primary hematological outpatient department

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16

Alati, Caterina, Bruno Martino, Antonio Marino, Francesca Ronco, Manuela Priolo, and Francesco Nobile. "Familial Chronic Myeloproliferative Neoplasms." Blood 116, no. 21 (2010): 3078. http://dx.doi.org/10.1182/blood.v116.21.3078.3078.

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Abstract Abstract 3078 Chronic myeloproliferative neoplasms (CMNs) include Polycythemia Vera (PV), Essential Thrombocythemia (ET), and Primary Myelofibrosis (PMF). So far limited studies of familial clusters of CMNs have been reported.Familial chronic myeloproliferative neoplasms are defined when in the same pedigree at least two relatives have CMNs. Familial CMNs should be distinguished from inherited disorders with Mendelian transmission, high penetrance and polyclonal haematopoiesis named ‘hereditary erythrocytosis' and ‘hereditary thrombocytosis'. Recently a 5- to 7-fold higher risk of MPN

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17

Vinogradova, O. Yu, A. L. Neverova, M. V. Chernikov, et al. "Characteristics of regional epidemiological indicators of chronic myeloproliferative neoplasms." Oncohematology 20, no. 2 (2025): 16–29. https://doi.org/10.17650/1818-8346-2025-20-2-16-29.

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Background. Information on the epidemiological picture of chronic myeloid leukemia (CML) and, especially, Ph– chronic myeloproliferative neoplasm (MPN) in Russia is very scarce, each regional population study is important for obtaining information on the diseases in general.Aim. To analyze the regional epidemiological parameters of the most common MPN over a long period of time (2012–2023).Materials and methods. Clinical and epidemiological, population, retrospective-prospective, observational study of CML and classical Ph– MPN (polycythemia vera, essential thrombocythemia, primary myelofibros

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18

Roszkowska, Anna Maria, Rossana Leanza, Emanuela Aragona, et al. "Retinal Vessel Analysis and Microvascular Abnormalities in Patients with Philadelphia-Negative Chronic Myeloproliferative Neoplasms." Journal of Clinical Medicine 13, no. 8 (2024): 2232. http://dx.doi.org/10.3390/jcm13082232.

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Background: Philadelphia-negative chronic myeloproliferative neoplasms are a group of clonal hematopoietic disorders including polycythemia vera, essential thrombocythemia, and primary myelofi-brosis. These neoplasms are characterized by an increased risk of thrombotic complications. Several studies have highlighted that the study of vessels of the retina offers the opportunity to visualize, in vivo, the damage to microcirculation that is common in various systemic pathologies. Methods: in our study, forty patients underwent an ophthalmological examination, using non-invasive imaging tech-niqu

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19

Jager, R., and R. Kralovics. "Molecular Pathogenesis of Philadelphia Chromosome Negative Chronic Myeloproliferative Neoplasms." Current Cancer Drug Targets 11, no. 1 (2011): 20–30. http://dx.doi.org/10.2174/156800911793743628.

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20

Yung, Yammy, Emily Lee, Hiu-Tung Chu, Pui-Kwan Yip, and Harinder Gill. "Targeting Abnormal Hematopoietic Stem Cells in Chronic Myeloid Leukemia and Philadelphia Chromosome-Negative Classical Myeloproliferative Neoplasms." International Journal of Molecular Sciences 22, no. 2 (2021): 659. http://dx.doi.org/10.3390/ijms22020659.

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Myeloproliferative neoplasms (MPNs) are unique hematopoietic stem cell disorders sharing mutations that constitutively activate the signal-transduction pathways involved in haematopoiesis. They are characterized by stem cell-derived clonal myeloproliferation. The key MPNs comprise chronic myeloid leukemia (CML), polycythemia vera (PV), essential thrombocythemia (ET), and primary myelofibrosis (PMF). CML is defined by the presence of the Philadelphia (Ph) chromosome and BCR-ABL1 fusion gene. Despite effective cytoreductive agents and targeted therapy, complete CML/MPN stem cell eradication is r

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21

Yung, Yammy, Emily Lee, Hiu-Tung Chu, Pui-Kwan Yip, and Harinder Gill. "Targeting Abnormal Hematopoietic Stem Cells in Chronic Myeloid Leukemia and Philadelphia Chromosome-Negative Classical Myeloproliferative Neoplasms." International Journal of Molecular Sciences 22, no. 2 (2021): 659. http://dx.doi.org/10.3390/ijms22020659.

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Myeloproliferative neoplasms (MPNs) are unique hematopoietic stem cell disorders sharing mutations that constitutively activate the signal-transduction pathways involved in haematopoiesis. They are characterized by stem cell-derived clonal myeloproliferation. The key MPNs comprise chronic myeloid leukemia (CML), polycythemia vera (PV), essential thrombocythemia (ET), and primary myelofibrosis (PMF). CML is defined by the presence of the Philadelphia (Ph) chromosome and BCR-ABL1 fusion gene. Despite effective cytoreductive agents and targeted therapy, complete CML/MPN stem cell eradication is r

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22

Urosevic, Ivana, Andrija Bogdanovic, and Danijela Lekovic. "Myeloproliferative neoplasms and pregnancy." Medical review 75, Suppl. 1 (2022): 121–26. http://dx.doi.org/10.2298/mpns22s1121u.

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Introduction. The Myeloproliferative Neoplasms are a heterogeneous group of clonal hematopoietic stem cell disorders characterized by increased proliferation of the myeloid lineages in the bone marrow. A particular clinical challenge is presented by certain situations in patients with myeloproliferative Neoplasms, which we do not encounter daily. For this reason, in this paper, we will emphasize the approach to overcoming obstacles in patients with Myeloproliferative Neoplasms in specific settings, like pregnancy. Pregnancy with Philadelphia chromosome-negative Myeloproliferative Neoplasms has

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23

Sabattini, Elena, Marco Pizzi, Claudio Agostinelli, et al. "Progression in Ph-Chromosome-Negative Myeloproliferative Neoplasms: An Overview on Pathologic Issues and Molecular Determinants." Cancers 13, no. 21 (2021): 5531. http://dx.doi.org/10.3390/cancers13215531.

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Progression in Ph-chromosome-negative myeloproliferative neoplasms (MPN) develops with variable incidence and time sequence in essential thrombocythemia, polycythemia vera, and primary myelofibrosis. These diseases show different clinic-pathologic features and outcomes despite sharing deregulated JAK/STAT signaling due to mutations in either the Janus kinase 2 or myeloproliferative leukemia or CALReticulin genes, which are the primary drivers of the diseases, as well as defined diagnostic criteria and biomarkers in most cases. Progression is defined by the development or worsening of marrow fi

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24

Guerin, Estelle, Francis Belloc, Gabriel Etienne, Pierre Duffau, Francois-Xavier Mahon, and Eric Lippert. "Reactive Oxygen Species Are Differentially Regulated in Chronic Myeloid Leukemia Versus Philadelphia Negative Myeloproliferative Neoplasms." Blood 112, no. 11 (2008): 4215. http://dx.doi.org/10.1182/blood.v112.11.4215.4215.

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Abstract Deregulation of tyrosine-kinases is a characteristic of most Myeloproliferative Neoplasms (MPN); evolution from chronic phase to acute leukemia depends on the acquisition of additional mutations. Reactive Oxygen Species (ROS), the production of which is increased by tyrosine-kinase activation, can be responsible for additional mutations. The role of ROS in generating genetic aberrations has been mainly studied in BCR-ABL-positive cell lines. Little is known of ROS metabolism in primary cells from CML or Philadelphia-negative MPN (Ph-MPN). After informed consent, cells from blood or bo

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25

Jelinek, Jaroslav, Yasuhiro Oki, Vazganush Gharibyan, et al. "JAK2 mutation 1849G>T is rare in acute leukemias but can be found in CMML, Philadelphia chromosome–negative CML, and megakaryocytic leukemia." Blood 106, no. 10 (2005): 3370–73. http://dx.doi.org/10.1182/blood-2005-05-1800.

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AbstractAn activating 1849G&gt;T mutation of JAK2 (Janus kinase 2) tyrosine kinase was recently described in chronic myeloproliferative disorders (MPDs). Its role in other hematologic neoplasms is unclear. We developed a quantitative pyrosequencing assay and analyzed 374 samples of hematologic neoplasms. The mutation was frequent in polycythemia vera (PV) (86%) and myelofibrosis (95%) but less prevalent in acute myeloid leukemia (AML) with an antecedent PV or myelofibrosis (5 [36%] of 14 patients). JAK2 mutation was also detected in 3 (19%) of 16 patients with Philadelphia-chromosome (Ph)–

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Treaba, Diana O., Salwa Khedr, Shamlal Mangray, Cynthia Jackson, Jorge J. Castillo, and Eric S. Winer. "Acute Myeloid Leukemia Evolving from JAK 2-Positive Primary Myelofibrosis and Concomitant CD5-Negative Mantle Cell Lymphoma: A Case Report and Review of the Literature." Case Reports in Hematology 2012 (2012): 1–6. http://dx.doi.org/10.1155/2012/875039.

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Primary myelofibrosis (formerly known as chronic idiopathic myelofibrosis), has the lowest incidence amongst the chronic myeloproliferative neoplasms and is characterized by a rather short median survival and a risk of progression to acute myeloid leukemia (AML) noted in a small subset of the cases, usually as a terminal event. As observed with other chronic myeloproliferative neoplasms, the bone marrow biopsy may harbor small lymphoid aggregates, often assumed reactive in nature. In our paper, we present a 70-year-old Caucasian male who was diagnosed with primary myelofibrosis, and after 8 ye

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27

Джумабаева, Болдукыз Толгонбаевна. "The Role of Leukocytes in the Formation of Neutrophil Extracellular Traps and Thrombosis in Ph-Negative Myeloproliferative Neoplasms: A Literature Review." Клиническая онкогематология 16, no. 3 (2023): 263–67. http://dx.doi.org/10.21320/2500-2139-2023-16-3-263-267.

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Thrombotic complications often cause death in patients with chronic Ph-negative myeloproliferative neoplasms (MPNs). In spite of numerous studies, the pathogenesis of thrombus formation in MPN patients remains unclear. Its mechanism is complex and is determined by many factors. One of the essential phases in thrombogenesis is characterized by the activation of cell mechanisms and formation of neutrophil extracellular traps (NETs). NETs consist of DNA strands, histones, granular proteins and along with pathogen destruction provide an ideal matrix for platelet and clotting mechanism activation.

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28

Pulido, Mariem, Elena Tuna Aguilar, and Junice Teresita Sosa Romero. "Association of Hyperuricemia with Thrombosis in Philadelphia-Negative Chronic Myeloproliferative Neoplasms." Blood 144, Supplement 1 (2024): 6636. https://doi.org/10.1182/blood-2024-203647.

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INTRODUCTION Elevation of uric acid (UA) in chronic myeloproliferative neoplasms (cMPN) has been attributed to an increase in production by clonal neoplasm cells and a decrease in its excretion due to a decreased glomerular filtration rate (GFR) [1]. A few studies have associated hyperuricemia with a higher risk of thrombosis in cMPN, comparing essential thrombocythemia (ET) and polycythemia vera (PV). Elevated levels of UA have been associated with a higher risk of cardiovascular morbidity and mortality. Thrombosis is a frequently encountered event in cMPN, mainly in polycythemia vera PV and

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Holmström, Morten Orebo, Hans Carl Hasselbalch, and Mads Hald Andersen. "Cancer Immune Therapy for Philadelphia Chromosome-Negative Chronic Myeloproliferative Neoplasms." Cancers 12, no. 7 (2020): 1763. http://dx.doi.org/10.3390/cancers12071763.

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Philadelphia chromosome-negative chronic myeloproliferative neoplasms (MPN) are neoplastic diseases of the hematopoietic stem cells in the bone marrow. MPN are characterized by chronic inflammation and immune dysregulation. Of interest, the potent immunostimulatory cytokine interferon-α has been used to treat MPN for decades. A deeper understanding of the anti-cancer immune response and of the different immune regulatory mechanisms in patients with MPN has paved the way for an increased perception of the potential of cancer immunotherapy in MPN. Therapeutic vaccination targeting the driver mut

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30

Barcelos, Michelle Maccarini, and Maria Cláudia Santos-Silva. "Molecular approach to diagnose BCR/ABL negative chronic myeloproliferative neoplasms." Revista Brasileira de Hematologia e Hemoterapia 33, no. 4 (2011): 290–96. http://dx.doi.org/10.5581/1516-8484.20110079.

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31

Виноградова, О. Ю., Анна Леонидовна Неверова, М. М. Панкрашкина, et al. "Paroxysmal Nocturnal Hemoglobinuria and Primary Myelofibrosis as an Extremely Rare Combination of Clonal Hematological Diseases: A Literature Review and Two Clinical Case Reports." Clinical Oncohematology 17, no. 2 (2024): 195–203. http://dx.doi.org/10.21320/2500-2139-2024-17-2-195-203.

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The combinations of paroxysmal nocturnal hemoglobinuria (PNH) and chronic myeloproliferative neoplasms (CMPNs) are extremely rare. All of them refer to clonal hematological diseases and are characterized by high thrombosis risk, which most commonly causes death. This paper provides literature data on 38 combined cases of PNH and Ph-negative/Ph-positive CMPNs mainly in the “case report” format, taken from 22 sources published in 1970–2022. Additionally, the paper reports personal experience with 2 combined cases of PNH and primary myelofibrosis (PMF/PNH) from the archive of the Moscow Municipal

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32

Sadigh, Sam, Robert P. Hasserjian, and Gabriela Hobbs. "Distinguishing atypical chronic myeloid leukemia from other Philadelphia-negative chronic myeloproliferative neoplasms." Current Opinion in Hematology 27, no. 2 (2020): 122–27. http://dx.doi.org/10.1097/moh.0000000000000565.

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33

Christensen, Alexander Sidelmann, Jonas Bech Møller, and Hans Carl Hasselbalch. "Chronic kidney disease in patients with the Philadelphia-negative chronic myeloproliferative neoplasms." Leukemia Research 38, no. 4 (2014): 490–95. http://dx.doi.org/10.1016/j.leukres.2014.01.014.

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34

Lasho, Terra, Ayalew Tefferi, Alessandro M. Vannucchi, et al. "LNK Mutation Studies In Chronic- and Blast-Phase Myeloproliferative Neoplasms and JAK2 Mutation-Negative Erythrocytosis." Blood 116, no. 21 (2010): 4105. http://dx.doi.org/10.1182/blood.v116.21.4105.4105.

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Abstract Abstract 4105 Background: JAK2 mutations are found in approximately 99% of patients with polycythemia vera (PV) and 60% of those with essential thrombocythemia (ET) or primary myelofibrosis (PMF). It is currently assumed that other mutations relevant to JAK signaling contribute to the pathogenesis of JAK2 mutation-negative myeloproliferative neoplasms (MPN). The same might hold true for some cases of “idiopathic erythrocytosis” associated with subnormal serum erythropoietin level (sEpo). LNK is a plasma membrane-bound adaptor protein whose function includes inhibition of wild-type and

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35

Torres, Dania G., Jhemerson Paes, Allyson G. da Costa, et al. "JAK2 Variant Signaling: Genetic, Hematologic and Immune Implication in Chronic Myeloproliferative Neoplasms." Biomolecules 12, no. 2 (2022): 291. http://dx.doi.org/10.3390/biom12020291.

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The JAK2V617F variant constitutes a genetic alteration of higher frequency in BCR/ABL1 negative chronic myeloproliferative neoplasms, which is caused by a substitution of a G ˃ T at position 1849 and results in the substitution of valine with phenylalanine at codon 617 of the polypeptide chain. Clinical, morphological and molecular genetic features define the diagnosis criteria of polycythemia vera, essential thrombocythemia and primary myelofibrosis. Currently, JAK2V617F is associated with clonal hematopoiesis, genomic instability, dysregulations in hemostasis and immune response. JAK2V617F c

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Masselli, Elena, Giulia Pozzi, Giuliana Gobbi, et al. "Cytokine Profiling in Myeloproliferative Neoplasms: Overview on Phenotype Correlation, Outcome Prediction, and Role of Genetic Variants." Cells 9, no. 9 (2020): 2136. http://dx.doi.org/10.3390/cells9092136.

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Among hematologic malignancies, the classic Philadelphia-negative chronic myeloproliferative neoplasms (MPNs) are considered a model of inflammation-related cancer development. In this context, the use of immune-modulating agents has recently expanded the MPN therapeutic scenario. Cytokines are key mediators of an auto-amplifying, detrimental cross-talk between the MPN clone and the tumor microenvironment represented by immune, stromal, and endothelial cells. This review focuses on recent advances in cytokine-profiling of MPN patients, analyzing different expression patterns among the three ma

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Swaminathan, Mahesh, Keyur P. Patel, Julie Huynh-Lu, et al. "Unique Case of Myeloproliferative Neoplasm with Two Rare Clonal Abnormalities: Rare JAK2 Exon 12 Mutation and Rare e14a3 (b3a3) BCR/ABL Fusion Transcript." Acta Haematologica 141, no. 1 (2018): 23–27. http://dx.doi.org/10.1159/000494427.

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Myeloproliferative neoplasms (MPNs) are clonal disorders divided into Philadelphia (Ph) chromosome-positive chronic myeloid leukemia (CML) or Ph chromosome-negative MPNs. Co-occurrence of these disease entities is very rare and typically involves presence of common p190 or p210 BCR/ABL fusion transcript (responsible for CML) along with JAK2V617F mutation (most common driver mutation in Ph-negative MPNs). Because of the rarity of such cases, it is not clear if the outcomes are any different in these patients. In this article, we report a unique patient with polycythemia vera driven by a rare co

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Cahill, Kirk, Anand Ashwin Patel, Hongtao Liu, et al. "Outcomes of IDH-Mutated Advanced Phase Ph-Negative Myeloproliferative Neoplasms Treated with IDH Inhibitors." Blood 134, Supplement_1 (2019): 4176. http://dx.doi.org/10.1182/blood-2019-122380.

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Background: Myeloproliferative neoplasms (MPNs) that progress to an accelerated phase (AP) or blast phase (BP) have poor outcomes with a median survival of 3 to 5 months. Approximately 20% of MPN-BP patients have a pathogenic mutation in IDH1 or IDH2. Ivosidenib and enasidenib, inhibitors of the IDH1 and IDH2 mutant enzymes respectively, provide a new treatment approach for high-risk IDH-mutated acute myeloid leukemia (AML). There are limited clinical trial data and real-world experience with IDH inhibitors in MPN-AP/BP. We hypothesized that patients with IDH-mutated MPN-AP/BP may benefit from

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Stuckey, Ruth, Cristina Bilbao-Sieyro, Adrián Segura-Díaz, and María Teresa Gómez-Casares. "Molecular Studies for the Early Detection of Philadelphia-Negative Myeloproliferative Neoplasms." International Journal of Molecular Sciences 24, no. 16 (2023): 12700. http://dx.doi.org/10.3390/ijms241612700.

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JAK2 V617F is the predominant driver mutation in patients with Philadelphia-negative myeloproliferative neoplasms (MPN). JAK2 mutations are also frequent in clonal hematopoiesis of indeterminate potential (CHIP) in otherwise “healthy” individuals. However, the period between mutation acquisition and MPN diagnosis (known as latency) varies widely between individuals, with JAK2 mutations detectable several decades before diagnosis and even from birth in some individuals. Here, we will review the current evidence on the biological factors, such as additional mutations and chronic inflammation, wh

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Rampal, Raajit K., Sean M. Devlin, Jay P. Patel, et al. "Integrated Genetic Profiling Of JAK2 Wildtype Chronic-Phase Myeloproliferative Neoplasms." Blood 122, no. 21 (2013): 1588. http://dx.doi.org/10.1182/blood.v122.21.1588.1588.

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Abstract Background The Myeloproliferative Neoplasms (MPNs), including Polycythemia Vera (PV), Essential Thrombocythemia (ET), and Primary Myelofibrosis (PMF) are clonal hematopoietic disorders. JAK2V617F mutations are observed in approximately 90-95% of PV cases, but only 40-50% of ET and PMF cases. Although JAK2 exon 12 and LNK mutations are observed in the majority of JAK2V617F-negative PV patients, candidate gene and exome sequencing studies to date have not identified activating oncogenes in the majority of JAK2V617F-negative ET/PMF patients. Thus, further genetic investigations are neede

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Hasselbalch, Hans Carl, Jean-Jacques Kiladjian, and Richard T. Silver. "Interferon Alfa in the Treatment of Philadelphia-Negative Chronic Myeloproliferative Neoplasms." Journal of Clinical Oncology 29, no. 18 (2011): e564-e565. http://dx.doi.org/10.1200/jco.2011.35.6238.

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Sørensen, Anders Lindholm, and Hans Carl Hasselbalch. "Antecedent cardiovascular disease and autoimmunity in Philadelphia-negative chronic myeloproliferative neoplasms." Leukemia Research 41 (February 2016): 27–35. http://dx.doi.org/10.1016/j.leukres.2015.11.017.

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Caramazza, Domenica, Clementina Caracciolo, Rita Barone, et al. "Correlation between leukocytosis and thrombosis in Philadelphia-negative chronic myeloproliferative neoplasms." Annals of Hematology 88, no. 10 (2009): 967–71. http://dx.doi.org/10.1007/s00277-009-0706-x.

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Skov, Vibe, Mads Thomassen, Lasse Kjær, Thomas Stauffer Larsen, Torben A. Kruse, and Hans Hasselbalch. "Highly Deregulated Fibulins in Patients with Philadelphia-Negative Chronic Myeloproliferative Neoplasms." Blood 134, Supplement_1 (2019): 5396. http://dx.doi.org/10.1182/blood-2019-130560.

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Introduction The Philadelphia-negative chronic myeloproliferative neoplasms (MPNs) develop in a biological continuum from the early cancer stages (ET/PV) to the advanced myelofibrosis stage characterized by huge splenomegaly, bone marrow failure and -fibrosis. Importantly, bone marrow fibrosis also increases from the early stages with reticulin fibrosis only and later deposition of mature collagen as well. Fibulins are glycoproteins that are important constituents of the extracellular matrix (ECM). Thus, fibulins have been shown to modulate cell morphology, growth, adhesion and motility. Dysre

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Oh, Stephen T., Jacob M. Zahn, Carol D. Jones, et al. "Identification of Novel LNK Mutations In Patients with Chronic Myeloproliferative Neoplasms and Related Disorders." Blood 116, no. 21 (2010): 315. http://dx.doi.org/10.1182/blood.v116.21.315.315.

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Abstract Abstract 315 Introduction: Dysregulated JAK-STAT signaling in chronic myeloproliferative neoplasms (MPNs) has primarily been attributed to activating mutations in tyrosine kinases. However, JAK-STAT activation can be demonstrated in some patients lacking JAK2 or MPL mutations, suggesting alteration of other regulatory elements in this pathway. One regulator of JAK-STAT signaling is LNK (SH2B3), an adapter protein that contains a proline-rich N-terminal dimerization domain (Pro/DD), a pleckstrin homology (PH) domain (plasma membrane localization), and an SH2 domain. LNK binds to cytoki

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Kiem, Dominik, Sandro Wagner, Teresa Magnes, Alexander Egle, Richard Greil, and Thomas Melchardt. "The Role of Neutrophilic Granulocytes in Philadelphia Chromosome Negative Myeloproliferative Neoplasms." International Journal of Molecular Sciences 22, no. 17 (2021): 9555. http://dx.doi.org/10.3390/ijms22179555.

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Philadelphia chromosome negative myeloproliferative neoplasms (MPN) are composed of polycythemia vera (PV), essential thrombocytosis (ET), and primary myelofibrosis (PMF). The clinical picture is determined by constitutional symptoms and complications, including arterial and venous thromboembolic or hemorrhagic events. MPNs are characterized by mutations in JAK2, MPL, or CALR, with additional mutations leading to an expansion of myeloid cell lineages and, in PMF, to marrow fibrosis and cytopenias. Chronic inflammation impacting the initiation and expansion of disease in a major way has been de

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Svidnicki, Maria Carolina Costa Melo, Paula De Melo Campos, Moisés Alves Ferreira Filho, et al. "Mutations in Triple-Negative Patients with Myeloproliferative Neoplasms." Blood 134, Supplement_1 (2019): 5395. http://dx.doi.org/10.1182/blood-2019-128764.

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Background Myeloproliferative neoplasms (MPNs) are chronic hematopoietic stem cell disorders, including polycythemia vera (PV), essential thrombocythemia (ET), and primary myelofibrosis (MF). JAK2, MPL, and CALR mutations are considered as "driver mutations" and are directly implicated in the disease pathogenesis by activation of JAK/STAT signaling. However, some patients do not harbor any of these mutations. Since such triple-negative MPNs are very rare, no specific molecular markers were established to use for a precise differential diagnosis yet. So far, the introduction of next generation

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Мисюрин, В. А., А. В. Мисюрин, Л. А. Кесаева та ін. "Новые маркеры прогрессирования хронического миелолейкоза". Clinical Oncohematology 7, № 2 (2014): 206–12. https://doi.org/10.21320/2500-2139-2014-7-2-206-212.

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In the contrast to Ph’-negative chronic myeloproliferative disorders (cMPD), chronic myelogenous leukemia (CML) is prone to rather early transformation into the later stage disease, known as the acceleration phase (AP) and blast crisis (BC). Myeloproliferative disorders are termed myeloproliferative neoplasms in the WHO classification, 2008. Molecular mechanisms underlying CML progression are unclear and still being studied. Recently, it was shown that progression of some malignancies was associated with activation and hyperexpression of some genes from the cancer-testis (CT) family. In this s

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Giraldo-Rincon, Ana Isabel, Sara Naranjo Molina, Natalia Gomez-Lopera, et al. "JAK2, CALR, and MPL Mutation Profiles in Colombian patients with BCR-ABL Negative Myeloproliferative Neoplasms." Colombia Medica 54, no. 3 (2023): e2035353. http://dx.doi.org/10.25100/cm.v54i3.5353.

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BackgroundAmong the chronic myeloproliferative neoplasms (MPNs) not associated with BCR-ABL mutations are polycythemia vera, primary myelofibrosis, and essential thrombocythemia. These diseases are caused by gene mutations, such as the JAK2, MPL, and CALR genes, which regulate the JAK-STAT signaling pathway. ObjectiveThis study aimed to establish the frequencies of mutations in the JAK2, MPL, and CALR genes in Colombian patients with a negative clinical diagnosis of BCR-ABL chronic myeloproliferative neoplasms. MethodsThe JAK2 V617F and MPL W515K mutations and deletions or insertions in exon 9

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Benedetti, Edoardo, Rita Tavarozzi, Riccardo Morganti, et al. "Organ Stiffness in the Work-Up of Myelofibrosis and Philadelphia-Negative Chronic Myeloproliferative Neoplasms." Journal of Clinical Medicine 9, no. 7 (2020): 2149. http://dx.doi.org/10.3390/jcm9072149.

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To define the role of spleen stiffness (SS) and liver stiffness (LS) in myelofibrosis and other Philadelphia (Ph)-negative myeloproliferative neoplasms (MPNs), we studied, by ultrasonography (US) and elastography (ES), 70 consecutive patients with myelofibrosis (MF) (no.43), essential thrombocythemia (ET) (no.10), and polycythemia vera (PV) (no.17). Overall, the median SS was not different between patients with MF and PV (p = 0.9); however, both MF and PV groups had significantly higher SS than the ET group (p = 0.011 and p = 0.035, respectively) and healthy controls (p < 0.0001 and p = 0.0

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